Asymptomatic Hemorrhagic Transformation of Infarction and Its Relationship With Functional Outcome and Stroke Subtype: Assessment From the Tinzaparin in Acute Ischaemic Stroke Trial
Asymptomatic hemorrhagic transformation of infarction (AHTI) is common, but its risk factors and relationship with functional outcome are poorly defined. The analyses used data from the Tinzapararin in Acute Ischaemic Stroke Trial, a randomized controlled trial assessing tinzaparin (low molecular we...
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| Veröffentlicht in: | Stroke (1970) 2010-12, Vol.41 (12), p.2834-2839 |
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| creator | ENGLAND, Timothy J BATH, Philip M. W BERND RINGELSTEIN, E SARE, Gillian M GEEGANAGE, Chamila MOULIN, Thierry O'NEILL, Desmond WOIMANT, France CHRISTENSEN, Hanne DE DEYN, Peter LEYS, Didier |
| description | Asymptomatic hemorrhagic transformation of infarction (AHTI) is common, but its risk factors and relationship with functional outcome are poorly defined.
The analyses used data from the Tinzapararin in Acute Ischaemic Stroke Trial, a randomized controlled trial assessing tinzaparin (low molecular weight heparin) versus aspirin in 1484 patients with acute ischemic stroke. CT head scans (baseline, day 10) were adjudicated for the presence of hemorrhagic transformation. Stroke subtype was classified according to modified Trial of Org 10172 in Acute Stroke Treatment (small vessel, large vessel, cardioembolic) and the Oxfordshire Community Stroke Project (total anterior, partial anterior, lacunar, and posterior circulatory syndromes). Modified Rankin scale and Barthel Index were measured at 3 and 6 months. Analyses were adjusted for age, sex, severity, blood pressure, infarct volume, and treatment. Symptomatic hemorrhage was excluded.
At day 10, AHTI did not differ between aspirin (300 mg; 32.8%) and medium-dose (100 IU/kg; 36.0%) and high-dose (175 IU/kg; 31.4%) tinzaparin groups (P = 0.44). Relative to lacunar stroke, AHTI on follow-up CT was significantly increased in total anterior circulation syndrome (odds ratio, 11.5; 95% CI, 7.1 to 18.7) and partial anterior circulation syndrome (odds ratio, 7.2; 95% CI, 4.5 to 11.4) stroke. Similarly, relative to small vessel disease, AHTI was increased in large vessel (odds ratio, 15.1; 95% CI, 9.4 to 24.3) and cardioembolic (odds ratio, 14.1; 95% CI, 8.5 to 23.5) stroke. After adjustment for infarct volume, the presence of AHTI was not associated with outcome at 3 or 6 months as measured by the modified Rankin Scale and Barthel Index.
AHTI is increased in ischemic stroke with cortical syndromes and of large vessel or cardioembolic etiology. Heparin does not increase AHTI. AHTI is not associated with functional outcome. |
| doi_str_mv | 10.1161/STROKEAHA.109.573063 |
| format | Article |
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The analyses used data from the Tinzapararin in Acute Ischaemic Stroke Trial, a randomized controlled trial assessing tinzaparin (low molecular weight heparin) versus aspirin in 1484 patients with acute ischemic stroke. CT head scans (baseline, day 10) were adjudicated for the presence of hemorrhagic transformation. Stroke subtype was classified according to modified Trial of Org 10172 in Acute Stroke Treatment (small vessel, large vessel, cardioembolic) and the Oxfordshire Community Stroke Project (total anterior, partial anterior, lacunar, and posterior circulatory syndromes). Modified Rankin scale and Barthel Index were measured at 3 and 6 months. Analyses were adjusted for age, sex, severity, blood pressure, infarct volume, and treatment. Symptomatic hemorrhage was excluded.
At day 10, AHTI did not differ between aspirin (300 mg; 32.8%) and medium-dose (100 IU/kg; 36.0%) and high-dose (175 IU/kg; 31.4%) tinzaparin groups (P = 0.44). Relative to lacunar stroke, AHTI on follow-up CT was significantly increased in total anterior circulation syndrome (odds ratio, 11.5; 95% CI, 7.1 to 18.7) and partial anterior circulation syndrome (odds ratio, 7.2; 95% CI, 4.5 to 11.4) stroke. Similarly, relative to small vessel disease, AHTI was increased in large vessel (odds ratio, 15.1; 95% CI, 9.4 to 24.3) and cardioembolic (odds ratio, 14.1; 95% CI, 8.5 to 23.5) stroke. After adjustment for infarct volume, the presence of AHTI was not associated with outcome at 3 or 6 months as measured by the modified Rankin Scale and Barthel Index.
AHTI is increased in ischemic stroke with cortical syndromes and of large vessel or cardioembolic etiology. Heparin does not increase AHTI. AHTI is not associated with functional outcome.</description><identifier>ISSN: 0039-2499</identifier><identifier>ISSN: 1524-4628</identifier><identifier>EISSN: 1524-4628</identifier><identifier>DOI: 10.1161/STROKEAHA.109.573063</identifier><identifier>PMID: 21030711</identifier><identifier>CODEN: SJCCA7</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Aged ; Anticoagulants - therapeutic use ; Aspirin - therapeutic use ; Biological and medical sciences ; Cerebral Hemorrhage - drug therapy ; Cerebral Hemorrhage - pathology ; Cerebral Infarction - drug therapy ; Cerebral Infarction - pathology ; Dose-Response Relationship, Drug ; Double-Blind Method ; Female ; Fibrinolytic Agents - therapeutic use ; Follow-Up Studies ; Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy ; Heparin, Low-Molecular-Weight - therapeutic use ; Humans ; Male ; Medical sciences ; Middle Aged ; Nervous system (semeiology, syndromes) ; Neurology ; Odds Ratio ; Platelet Aggregation Inhibitors - therapeutic use ; Risk Factors ; Stroke - drug therapy ; Stroke - pathology ; Tomography, X-Ray Computed ; Treatment Outcome ; Vascular diseases and vascular malformations of the nervous system</subject><ispartof>Stroke (1970), 2010-12, Vol.41 (12), p.2834-2839</ispartof><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c317t-7ca80b0514539cb22ee13542f8a2cd8cd4d9073f282bcbec9c584af48eb141c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3674,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23652395$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21030711$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>ENGLAND, Timothy J</creatorcontrib><creatorcontrib>BATH, Philip M. W</creatorcontrib><creatorcontrib>BERND RINGELSTEIN, E</creatorcontrib><creatorcontrib>SARE, Gillian M</creatorcontrib><creatorcontrib>GEEGANAGE, Chamila</creatorcontrib><creatorcontrib>MOULIN, Thierry</creatorcontrib><creatorcontrib>O'NEILL, Desmond</creatorcontrib><creatorcontrib>WOIMANT, France</creatorcontrib><creatorcontrib>CHRISTENSEN, Hanne</creatorcontrib><creatorcontrib>DE DEYN, Peter</creatorcontrib><creatorcontrib>LEYS, Didier</creatorcontrib><creatorcontrib>TAIST Investigators</creatorcontrib><title>Asymptomatic Hemorrhagic Transformation of Infarction and Its Relationship With Functional Outcome and Stroke Subtype: Assessment From the Tinzaparin in Acute Ischaemic Stroke Trial</title><title>Stroke (1970)</title><addtitle>Stroke</addtitle><description>Asymptomatic hemorrhagic transformation of infarction (AHTI) is common, but its risk factors and relationship with functional outcome are poorly defined.
The analyses used data from the Tinzapararin in Acute Ischaemic Stroke Trial, a randomized controlled trial assessing tinzaparin (low molecular weight heparin) versus aspirin in 1484 patients with acute ischemic stroke. CT head scans (baseline, day 10) were adjudicated for the presence of hemorrhagic transformation. Stroke subtype was classified according to modified Trial of Org 10172 in Acute Stroke Treatment (small vessel, large vessel, cardioembolic) and the Oxfordshire Community Stroke Project (total anterior, partial anterior, lacunar, and posterior circulatory syndromes). Modified Rankin scale and Barthel Index were measured at 3 and 6 months. Analyses were adjusted for age, sex, severity, blood pressure, infarct volume, and treatment. Symptomatic hemorrhage was excluded.
At day 10, AHTI did not differ between aspirin (300 mg; 32.8%) and medium-dose (100 IU/kg; 36.0%) and high-dose (175 IU/kg; 31.4%) tinzaparin groups (P = 0.44). Relative to lacunar stroke, AHTI on follow-up CT was significantly increased in total anterior circulation syndrome (odds ratio, 11.5; 95% CI, 7.1 to 18.7) and partial anterior circulation syndrome (odds ratio, 7.2; 95% CI, 4.5 to 11.4) stroke. Similarly, relative to small vessel disease, AHTI was increased in large vessel (odds ratio, 15.1; 95% CI, 9.4 to 24.3) and cardioembolic (odds ratio, 14.1; 95% CI, 8.5 to 23.5) stroke. After adjustment for infarct volume, the presence of AHTI was not associated with outcome at 3 or 6 months as measured by the modified Rankin Scale and Barthel Index.
AHTI is increased in ischemic stroke with cortical syndromes and of large vessel or cardioembolic etiology. Heparin does not increase AHTI. AHTI is not associated with functional outcome.</description><subject>Aged</subject><subject>Anticoagulants - therapeutic use</subject><subject>Aspirin - therapeutic use</subject><subject>Biological and medical sciences</subject><subject>Cerebral Hemorrhage - drug therapy</subject><subject>Cerebral Hemorrhage - pathology</subject><subject>Cerebral Infarction - drug therapy</subject><subject>Cerebral Infarction - pathology</subject><subject>Dose-Response Relationship, Drug</subject><subject>Double-Blind Method</subject><subject>Female</subject><subject>Fibrinolytic Agents - therapeutic use</subject><subject>Follow-Up Studies</subject><subject>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</subject><subject>Heparin, Low-Molecular-Weight - therapeutic use</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Nervous system (semeiology, syndromes)</subject><subject>Neurology</subject><subject>Odds Ratio</subject><subject>Platelet Aggregation Inhibitors - therapeutic use</subject><subject>Risk Factors</subject><subject>Stroke - drug therapy</subject><subject>Stroke - pathology</subject><subject>Tomography, X-Ray Computed</subject><subject>Treatment Outcome</subject><subject>Vascular diseases and vascular malformations of the nervous system</subject><issn>0039-2499</issn><issn>1524-4628</issn><issn>1524-4628</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc2O0zAQgCMEYrsLb4CQL4hTin8Tm1u02m4rVqq0jcQxcpwJCcRxsJ1DeS_ej2xbliOSJdsz34xH_pLkHcFrQjLy6VA-7r_cFdtiTbBai5zhjL1IVkRQnvKMypfJCmOmUsqVukquQ_iOMaZMitfJFSWY4ZyQVfK7CEc7RWd17A3agnXed_rbci69HkPr_FPGjci1aDe22pvTTY8N2sWAHmE4pUPXT-hrHzu0mccToge0n6NxFk7wIXr3A9BhruNxgs-oCAFCsDBGtPHOotgBKvvxl56070e0rMLMEdAumE6DXea5dCh9r4c3yatWDwHeXvabpNzclbfb9GF_v7stHlLDSB7T3GiJaywIF0yZmlIAwgSnrdTUNNI0vFE4Zy2VtDY1GGWE5LrlEmrCiWE3ycdz28m7nzOEWNk-GBgGPYKbQ6UEzzCTy6_-j5QUK5FTyRaSn0njXQge2mryvdX-WBFcPYmtnsUuEVWdxS5l7y8PzLWF5rnor8kF-HABdDB6aBd7pg__OJYJypRgfwCRErBd</recordid><startdate>20101201</startdate><enddate>20101201</enddate><creator>ENGLAND, Timothy J</creator><creator>BATH, Philip M. W</creator><creator>BERND RINGELSTEIN, E</creator><creator>SARE, Gillian M</creator><creator>GEEGANAGE, Chamila</creator><creator>MOULIN, Thierry</creator><creator>O'NEILL, Desmond</creator><creator>WOIMANT, France</creator><creator>CHRISTENSEN, Hanne</creator><creator>DE DEYN, Peter</creator><creator>LEYS, Didier</creator><general>Lippincott Williams & Wilkins</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>7TK</scope></search><sort><creationdate>20101201</creationdate><title>Asymptomatic Hemorrhagic Transformation of Infarction and Its Relationship With Functional Outcome and Stroke Subtype: Assessment From the Tinzaparin in Acute Ischaemic Stroke Trial</title><author>ENGLAND, Timothy J ; BATH, Philip M. W ; BERND RINGELSTEIN, E ; SARE, Gillian M ; GEEGANAGE, Chamila ; MOULIN, Thierry ; O'NEILL, Desmond ; WOIMANT, France ; CHRISTENSEN, Hanne ; DE DEYN, Peter ; LEYS, Didier</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c317t-7ca80b0514539cb22ee13542f8a2cd8cd4d9073f282bcbec9c584af48eb141c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Aged</topic><topic>Anticoagulants - therapeutic use</topic><topic>Aspirin - therapeutic use</topic><topic>Biological and medical sciences</topic><topic>Cerebral Hemorrhage - drug therapy</topic><topic>Cerebral Hemorrhage - pathology</topic><topic>Cerebral Infarction - drug therapy</topic><topic>Cerebral Infarction - pathology</topic><topic>Dose-Response Relationship, Drug</topic><topic>Double-Blind Method</topic><topic>Female</topic><topic>Fibrinolytic Agents - therapeutic use</topic><topic>Follow-Up Studies</topic><topic>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</topic><topic>Heparin, Low-Molecular-Weight - therapeutic use</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Nervous system (semeiology, syndromes)</topic><topic>Neurology</topic><topic>Odds Ratio</topic><topic>Platelet Aggregation Inhibitors - therapeutic use</topic><topic>Risk Factors</topic><topic>Stroke - drug therapy</topic><topic>Stroke - pathology</topic><topic>Tomography, X-Ray Computed</topic><topic>Treatment Outcome</topic><topic>Vascular diseases and vascular malformations of the nervous system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>ENGLAND, Timothy J</creatorcontrib><creatorcontrib>BATH, Philip M. W</creatorcontrib><creatorcontrib>BERND RINGELSTEIN, E</creatorcontrib><creatorcontrib>SARE, Gillian M</creatorcontrib><creatorcontrib>GEEGANAGE, Chamila</creatorcontrib><creatorcontrib>MOULIN, Thierry</creatorcontrib><creatorcontrib>O'NEILL, Desmond</creatorcontrib><creatorcontrib>WOIMANT, France</creatorcontrib><creatorcontrib>CHRISTENSEN, Hanne</creatorcontrib><creatorcontrib>DE DEYN, Peter</creatorcontrib><creatorcontrib>LEYS, Didier</creatorcontrib><creatorcontrib>TAIST Investigators</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Neurosciences Abstracts</collection><jtitle>Stroke (1970)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>ENGLAND, Timothy J</au><au>BATH, Philip M. W</au><au>BERND RINGELSTEIN, E</au><au>SARE, Gillian M</au><au>GEEGANAGE, Chamila</au><au>MOULIN, Thierry</au><au>O'NEILL, Desmond</au><au>WOIMANT, France</au><au>CHRISTENSEN, Hanne</au><au>DE DEYN, Peter</au><au>LEYS, Didier</au><aucorp>TAIST Investigators</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Asymptomatic Hemorrhagic Transformation of Infarction and Its Relationship With Functional Outcome and Stroke Subtype: Assessment From the Tinzaparin in Acute Ischaemic Stroke Trial</atitle><jtitle>Stroke (1970)</jtitle><addtitle>Stroke</addtitle><date>2010-12-01</date><risdate>2010</risdate><volume>41</volume><issue>12</issue><spage>2834</spage><epage>2839</epage><pages>2834-2839</pages><issn>0039-2499</issn><issn>1524-4628</issn><eissn>1524-4628</eissn><coden>SJCCA7</coden><abstract>Asymptomatic hemorrhagic transformation of infarction (AHTI) is common, but its risk factors and relationship with functional outcome are poorly defined.
The analyses used data from the Tinzapararin in Acute Ischaemic Stroke Trial, a randomized controlled trial assessing tinzaparin (low molecular weight heparin) versus aspirin in 1484 patients with acute ischemic stroke. CT head scans (baseline, day 10) were adjudicated for the presence of hemorrhagic transformation. Stroke subtype was classified according to modified Trial of Org 10172 in Acute Stroke Treatment (small vessel, large vessel, cardioembolic) and the Oxfordshire Community Stroke Project (total anterior, partial anterior, lacunar, and posterior circulatory syndromes). Modified Rankin scale and Barthel Index were measured at 3 and 6 months. Analyses were adjusted for age, sex, severity, blood pressure, infarct volume, and treatment. Symptomatic hemorrhage was excluded.
At day 10, AHTI did not differ between aspirin (300 mg; 32.8%) and medium-dose (100 IU/kg; 36.0%) and high-dose (175 IU/kg; 31.4%) tinzaparin groups (P = 0.44). Relative to lacunar stroke, AHTI on follow-up CT was significantly increased in total anterior circulation syndrome (odds ratio, 11.5; 95% CI, 7.1 to 18.7) and partial anterior circulation syndrome (odds ratio, 7.2; 95% CI, 4.5 to 11.4) stroke. Similarly, relative to small vessel disease, AHTI was increased in large vessel (odds ratio, 15.1; 95% CI, 9.4 to 24.3) and cardioembolic (odds ratio, 14.1; 95% CI, 8.5 to 23.5) stroke. After adjustment for infarct volume, the presence of AHTI was not associated with outcome at 3 or 6 months as measured by the modified Rankin Scale and Barthel Index.
AHTI is increased in ischemic stroke with cortical syndromes and of large vessel or cardioembolic etiology. Heparin does not increase AHTI. AHTI is not associated with functional outcome.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>21030711</pmid><doi>10.1161/STROKEAHA.109.573063</doi><tpages>6</tpages></addata></record> |
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| ispartof | Stroke (1970), 2010-12, Vol.41 (12), p.2834-2839 |
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| source | MEDLINE; American Heart Association Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection; Journals@Ovid Complete |
| subjects | Aged Anticoagulants - therapeutic use Aspirin - therapeutic use Biological and medical sciences Cerebral Hemorrhage - drug therapy Cerebral Hemorrhage - pathology Cerebral Infarction - drug therapy Cerebral Infarction - pathology Dose-Response Relationship, Drug Double-Blind Method Female Fibrinolytic Agents - therapeutic use Follow-Up Studies Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy Heparin, Low-Molecular-Weight - therapeutic use Humans Male Medical sciences Middle Aged Nervous system (semeiology, syndromes) Neurology Odds Ratio Platelet Aggregation Inhibitors - therapeutic use Risk Factors Stroke - drug therapy Stroke - pathology Tomography, X-Ray Computed Treatment Outcome Vascular diseases and vascular malformations of the nervous system |
| title | Asymptomatic Hemorrhagic Transformation of Infarction and Its Relationship With Functional Outcome and Stroke Subtype: Assessment From the Tinzaparin in Acute Ischaemic Stroke Trial |
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